Thursday, May 29, 2014

Basal Ganglia Implicated in Chronic Fatigue Syndrome

This study by Andrew Miller (see below) builds on previous work by Chaudhuri (Chaudhuri and Behan, 2000, Chaudhuri et al., 2003) and by Unger et al. (2012) linking fatigue to the basal ganglia in patients with ME/CFS.

The basal ganglia are a collection of nuclei found on both sides of the thalamus, outside and above the limbic system. Among other things, the basal ganglia control automatic coordinated activity (such as riding a bike or walking), eye movements, and reward circuits. Damage to this area would not only produce fatigue, but would account for the nystagmus (quick involuntary eye movements) as well as difficulty walking found in so many ME/CFS patients.

Brain imaging reveals clues about chronic fatigue syndrome

Eurekalert, May 23, 2014

A brain imaging study shows that patients with chronic fatigue syndrome may have reduced responses, compared with healthy controls, in a region of the brain connected with fatigue. The findings suggest that chronic fatigue syndrome is associated with changes in the brain involving brain circuits that regulate motor activity and motivation.

Compared with healthy controls, patients with chronic fatigue syndrome had less activation of the basal ganglia, as measured by fMRI (functional magnetic resonance imaging). This reduction of basal ganglia activity was also linked with the severity of fatigue symptoms.

According to the Centers for Disease Control and Prevention, chronic fatigue syndrome is a debilitating and complex disorder characterized by intense fatigue that is not improved by bed rest and that may be worsened by exercise or mental stress.

The results are scheduled for publication in the journal PLOS One.

"We chose the basal ganglia because they are primary targets of inflammation in the brain," says lead author Andrew Miller, MD. "Results from a number of previous studies suggest that increased inflammation may be a contributing factor to fatigue in CFS patients, and may even be the cause in some patients."

Miller is William P. Timmie professor of psychiatry and behavioral sciences at Emory University School of Medicine. The study was a collaboration among researchers at Emory University School of Medicine, the CDC's Chronic Viral Diseases Branch, and the University of Modena and Reggio Emilia in Italy. The study was funded by the CDC.

The basal ganglia are structures deep within the brain, thought to be responsible for control of movements and responses to rewards as well as cognitive functions. Several neurological disorders involve dysfunction of the basal ganglia, including Parkinson's disease and Huntington's disease, for example.

In previous published studies by Emory researchers, people taking interferon alpha as a treatment for hepatitis C, which can induce severe fatigue, also show reduced activity in the basal ganglia. Interferon alpha is a protein naturally produced by the body, as part of the inflammatory response to viral infection. Inflammation has also been linked to fatigue in other groups such as breast cancer survivors.

"A number of previous studies have suggested that responses to viruses may underlie some cases of CFS," Miller says. "Our data supports the idea that the body's immune response to viruses could be associated with fatigue by affecting the brain through inflammation. We are continuing to study how inflammation affects the basal ganglia and what effects that has on other brain regions and brain function. These future studies could help inform new treatments."

Treatment implications might include the potential utility of medications to alter the body's immune response by blocking inflammation, or providing drugs that enhance basal ganglia function, he says.

The researchers compared 18 patients diagnosed with chronic fatigue syndrome with 41 healthy volunteers. The 18 patients were recruited [not referred] based on an initial telephone survey followed by extensive clinical evaluations. The clinical evaluations, which came in two phases, were completed by hundreds of Georgia residents. People with major depression or who were taking antidepressants were excluded from the imaging study, although those with anxiety disorders were not.

For the brain imaging portion of the study, participants were told they'd win a dollar if they correctly guessed whether a preselected card was red or black. After they made a guess, the color of the card was revealed, and at that point researchers measured blood flow to the basal ganglia.

The key measurement was: how big is the difference in activity between a win or a loss?

Participants' scores on a survey gauging their levels of fatigue were tied to the difference in basal ganglia activity between winning and losing. Those with the most fatigue had the smallest changes, especially in the right caudate and the right globus pallidus, both parts of the basal ganglia.

Ongoing studies at Emory are further investigating the impact of inflammation on the basal ganglia, including studies using anti-inflammatory treatments to reduce fatigue and loss of motivation in patients with depression and other disorders with inflammation including cancer.

Monday, May 26, 2014

New Diagnostic Tools for ME/CFS

An article appeared recently in Deseret News describing the development of a biomarker for ME/CFS. The Lights believe they have found one based on gene expression (see below).

This is just one of several articles that has been published within the last few weeks about a possible biomarker for ME/CFS. Dr. Sonya Marshall-Gradisnik at Grifffith University in Australia says her team is on the cusp of a breakthrough for a biomarker. And, based on the recent neuroinflammation study by Yasuhito Nakatomi et al. in Japan, PET scans are also being considered. In the meantime, Dr. Betsy Keller has shown, yet again, that ME/CFS patients show unique responses to a 2-day CPET. She believes the test can serve as a diagnostic tool.

Between these efforts, we have no less than four proposed biomarkers: one genetic, one based on immune abnormalities, one neurological, and one arising from exercise intolerance. It will be interesting to see whether the IOM takes any of these into account. Even more to the point, will the P2P panel, which is currently examining the research definition of ME/CFS for the NIH, pay any attention to the principal areas of ME/CFS research?

Sufferers of chronic fatigue, fibromyalgia have hope in new diagnostic tool

By Wendy Leonard, Deseret News, May 16 2014

Alan and Kathleen Light

SALT LAKE CITY — Matt Remes moved with his family to Utah to pursue his dreams of becoming an Olympic skier.

But before he even got here, his body was making other plans.

Doctors don't know what happened to the now 15-year-old Park City student, but it has been decided that Remes suffers with chronic fatigue syndrome, an illness that is not very well understood but is keeping him from doing things other teenage boys can do — even those who are characteristically resilient and exceptionally competitive, like Remes.

"I was just so tired, and I couldn't understand why," said Remes, whose knobby knees and skinny ankles resemble those of someone half his age.

Fortunately for him and the more than 1 million sufferers of the largely unrecognized illness in the United States, a husband and wife team of researchers at the University of Utah has found a way to objectively explain it.

Using relatively new gene expression technology, Alan and Kathleen Light have discovered that certain genes react to physical exertion in different ways for people with chronic fatigue syndrome or fibromyalgia. Both are illnesses in which the body can't perform to its previously healthy capacity. It tires much more quickly and sometimes exhibits horrible pain.

"Fatigue is one of the most important homeostatic mechanisms in the body," said Alan Light. "Fatigue is there to prevent you from using up your energy source" and ultimately preserve muscles, which help to control the body's functions.

"It's very important to not use up your energy source," he said, adding that people go to great lengths to avoid fatigue — using an elevator to go up one floor, driving around a parking lot to find the closest parking spot, and putting off long meetings or conferences.

"Fatigue is the omnipresent phenomenon that we all have, and it really does control your life," he said.

Alan Light has been studying fatigue for decades, but teamed up 10 years ago with his wife, who has been working on understanding fibromyalgia and pain. Their latest findings are part of a National Institutes of Health study involving about 140 patients with chronic fatigue syndrome in Utah.

The mechanism for obtaining a gene expression profile from patients is already patented by the university, as there is hope to turn it into an actual diagnostic tool all doctors can use to confirm what is going on in someone's body.

Kathleen Light said it is important that people who suffer from these now-documented conditions get the help they need.

"In many ways, they have had their lives stolen from them," she said. "They feel they can't function doing their occupation, or in their family roles. Their lives are just completely turned upside down from this."

Patients were asked to perform a moderate exercise challenge and have their blood drawn before and several times after the activity. When compared to the performance of healthy individuals, genetic differences were readily apparent.

Angela Linford, of Holladay, has both chronic fatigue syndrome and fibromyalgia symptoms that appeared years ago when she was training heavily for a marathon. She said she has days when she can only handle crawling to the bathroom when absolutely necessary, and she has given up almost all of the physical activities she once loved.

Read the rest of this article here. (Note: There are two pages)

Wednesday, May 21, 2014

CDC AND NIH Officials Discussed "Desirable Outcome" of Seeing A Distinct Illness "Evaporate”

Reprinted with permission.

CFS Report Op/Ed, March 2014

By Craig Maupin 

In recent months, efforts to redefine chronic fatigue syndrome (CFS) have come under much scrutiny. The attention on the new definition should come as no surprise. Definitions and labels can be abused to direct research and clinical outcomes toward personal beliefs of authors. In the case of CFS, it has been easy, and perhaps necessary, for the DHHS to dismiss such past problems as unfounded speculation.

The truth is far more complex. In a document obtained by the CFS Report (see links below), Stephen E. Straus, widely known as the creator of the “fatigue syndrome” concept, discussed his hopes for 1994 redefinition of CFS with the CDC's Keiji Fukuda. The Straus/Fukuda letter, written after the submission of the new definition for publication, is frank. Straus predicts the new definition would cause “the notion of a discrete fatigue illness” to “evaporate”. 

Once a concept of a distinct disease evaporates, Straus claims a framework of idiopathic fatigue – a symptom that falls short of a distinct disease –  would be left behind. Straus predicts the new definition may lead to the “entire abandonment” of CFS. It is a strange prediction, to champion a definition that leads to the future abandonment, evaporation, and discrediting of that which one claims to want to define.

More remarkably, many attributions and beliefs in the Straus/Fukuda letter can be seen in current NIH peer review policies, conferences, and RFAs. Straus was often known to assert that research on immunological findings in subsets of CFS patients was/is "dubious," while praising researchers/papers focused on mind-body interaction. Straus also claimed CFS's pathology was "akin to pain", which has a "locus in the brain".

Today, grants for CFS are reviewed by reviewers who predominantly work in areas related to hypersensitivity to pain, with scores delivered by reviewers among a group of pain "oversensitivity" syndromes.

Like the Straus/Fukuda letter, RFAs and funding requests from the NIH also emphasize the brain and pain, while deemphasizing immunological findings. No mention of recent CFS research on autoimmunity, B cells, or antibodies is found in NIH funding requests. The current RFA (PAR 12-032) encourages CFS grant proposals fit seven categories the NIH terms as applicable to CFS:  aging and fatigue (NIA), alcoholism and fatigue (NIAAA), pelvic pain disorders (NIDCR/NIDDK), NIAID (unspecified, but immunologic mention seems purged from the current RFA), the brain (NINDS), behavioral relationships to fatigue (NINR), and mind/body interaction (NICAM). Terrell Hoffeld, who oversaw CFS peer review, seemed to reiterate attributions in the Straus/Fukuda letter when he told me that CFS had "moved on" from immunological research, and that relieving pain and anxiety from a neurological/brain approach was his goal at the CSR. (See: Scientific Review, CFS, and the NIH - The CFS Special Emphasis Panel.)

Straus admits that his integrative "fatigue syndrome" concept is not seen by some as “worthy of study”. Years later, his words seem eerily prophetic. Funding support for CFS is among the lowest of categorized diseases at the NIH.

Straus viewed CFS as predominantly a women's illness (NIH Publication No. 91-3059). Studies have shown women are less likely to be viewed as having a disease than a subjective complaint by doctors (Arber 2006). Straus, himself a clinician, suggests to Fukuda that CFS is an “impression on the part of the patient or physician that such a complaint is important.” Such attributions seem to represent a traditional mindset toward women's medical issues. Women are also more likely to be seen as having their symptoms originate in the brain or from psychological causes (Hoffman, Tarzian, 2001). Straus displays a disdain for CFS models that fail to revolve around an unnamed "locus in the brain."

Whether the DHHS acknowledges it or not, attributions seen in the letter between Straus/Fukuda laid much of the foundation for how the NIH handles emerging illnesses that predominantly affect women, such as CFS. Conferences sponsored by Drs. Vivian Pinn and Lawrence Tabak for CFS sought to interfuse pain, the concept of hypersensitivity to symptoms, and central processing in the brain into efforts to direct scientific research for CFS. Dr. Eleanor Hanna, constantly reiterated that grant proposals seen as "bad science" would not be considered fundable by ICs, and her views on CFS were well known within the ORWH and among Trans-NIH Working Group members (see link below). When the NIH continually ignores recent findings on B cells, unique antibodies and immune markers, and autoimmunity in its conferences, RFAs, and grant reviews, the foundation left by Straus seems not far behind.

Straus advocated the idea within the NIH shortly after CFS was first defined that negative studies for Epstein-Barr and known viruses were broad enough to scientifically disprove a viral or immunological pathology. However, some past DHHS leaders, such as Donna Dean and Philip Lee have pushed the HHS to acknowledge hundreds of peer reviewed papers documenting immunological defects in subsets of CFS. A definition of CFS on the ORWH website seems to suggest a more distinctive illness than Straus' definition. Perhaps such efforts suggest that some in HHS realize the definition and label created by Straus was never meant to be a benign search for scientific truth.

This disease possesses clear, distinct, and definable traits seen in no other illness: severe post-exertional collapse, flu-like symptoms, and orthostatic intolerance. Unlike many illnesses, the disease often is preceded by an acute viral infection. Without a definition and label that puts these distinct and unique symptoms at the forefront, HHS is simply striving to cling to one man’s "desired outcome" for the “evaporation” of a severe disease.  

Defining and labeling any illness, if done poorly, can do permanent damage. Fifty scientific experts know it. The sufferers and families and of those who suffer from CFS know it. And much of the scrutiny on the definition of CFS and current efforts of the IOM to revise the definition for CFS stem from historical and clear evidence that personal attributions played a role in the "evaporation" and "abandonment" of a devastating disease.

Straus/Fukuda DiscussEffects of Definition Chronic Fatigue Syndrome1

Straus/FukudaDiscuss Effects of Definition of Chronic Fatigue Syndrome2

Hanna NIH CFS WorkingGroup

Saturday, May 17, 2014

May 12th, 2014 - Reports from the San Francisco and Washington, DC Demos

San Francisco, CA - Federal Building/McKesson Plaza

May 12th was an unusually hot day. But that did not deter seventeen demonstrators - patients, friends, and supporters -  from gathering in front of the Federal Building on Seventh Street in San Francisco, where the regional HHS office is headquartered. 

The demonstration was scheduled to begin at noon, and within a few minutes of arriving, the group had set up six wheelchairs, erected banners, held up signs, arranged flowers, and displayed the photos of 11 people whose lives had been taken by ME. Susan Kreutzer passed out blue ribbons that she had made herself, and we pinned them to our clothing.

Nobody needed to be told what to do. The entire group acted in concert, with a smooth efficiency that belied the fact that most of us were strangers to one another.

After a short introductory speech, six of the demonstrators lined up behind the wheelchairs and read aloud the obituaries of those whose portraits were displayed.

While the obituaries were being read, the group stood quietly, listening in silence as the too short lives of these brave individuals were read. The youngest was David, age 17. The oldest was Tom Hennessy, 49, founder of May 12 International ME/CFS Awareness Day and a fierce advocate for patient rights. Tom's picture was displayed in the first wheelchair by itself. Also shown were photos of Allison Hunter (19), Lynn Gilderdale (31), Patrick Kelly (42), Casey Fero (23), Eric Moore (46), Amberlin Wu (29), Sophia Mirza (32), Emily Rose Collingridge (30), and Tracey Ash (26).

Afterwards, I entered the Federal Building with Jane Pannell to deliver two petitions demanding the cancellation of the IOM contract and the immediate adoption of the Canadian Consensus Criteria for ME. The petitions, totaling nearly 10,000 signatures, were given to HHS and to Nancy Pelosi's office, where I spoke with her long-time aide.

  • I explained why the IOM contract should be canceled, and gave her the experts' letter as well as a fact sheet with important information about ME/CFS, a request for legislative action to increase funding for scientific research, and a request that the misleading name “chronic fatigue syndrome” be replaced with Myalgic Encephalomyelitis.

Then we packed up, and repeated the demonstration a few blocks away at McKesson Plaza, where Senator Dianne Feinstein's office is located. One quick-thinking member of the group went into the building to fetch Senator Feinstein's aide, who came down to watch the demonstration. We spoke with him about the gravity of the illness, and delivered the two petitions, the experts' letter to Secretary Sebelius calling for the cancellation of the IOM contract, and a 55-page list of people who had died of ME. I handed him a copy of the obituaries the group had read.

Our message was loud and clear: "There are a million of us. We are dying of this disease. We've had 30 years of neglect from HHS, we are citizens, and we vote. It's time our representatives did their jobs and represented us!" 

What was most impressive about the demonstration was the degree to which people were willing to step up to the mat. When I asked, "Who wants to come with me to Nancy Pelosi's office and HHS?" every person there stepped forward. (The guards would only let two people in, unfortunately.) There was no question that if we had been allowed, all 17 of us would have marched into the Federal Building that day.

This may not have been the largest, but it was one of the most inspiring political events I have ever attended.

I want to give my profound thanks to everyone who came, as well as to all those who couldn't attend but expressed their support through donations, or by simply cheering us on. It buoyed us to know that you were all there in spirit.

Washington, DC - Capitol Building
The Banner of Hope

On the other side of the country, Mary Dimmock was busy setting up a May 12 demonstration at the Capitol Building. This year marks the 30-year anniversary of the Incline Village outbreak that saddled our community with the name "chronic fatigue syndrome"; the theme of the demonstration was "30 Years of Neglect."

Mary and two supporters, Marty Shore and Jim Mills, each of whom has a family member ill with ME/CFS, spread the Banner of Hope on the lawn. The Banner of Hope is a 65-foot long assembly of pillow case tops, each one of which has the name and dates of illness of a person bedridden with ME/CFS.

The Banner provides a moving testament to the toll this disease takes on the people it strikes. The demonstrators also displayed a banner with the portraits and obituaries of people who have died of ME/CFS.Two reporters, one from Televisa's Washington office and one from Medill News Service, came by to cover the event, and to arrange an interview with Mary. As Mary said, "Two leads is a very good thing."

Mary speaks with a reporter
Of the demonstration, Mary said, "There were mostly tourists there that day, but one person took a handout and said, 'I think this is the disease my daughter-in-law has!'

Giving even one person such a valuable piece of information was worth it."

Sunday, May 11, 2014

All in the mind? Why critics are wrong to deny the existence of chronic fatigue syndrome

Below is an article which appeared two years ago in the Daily Mail Online (UK). In this article Sonia Poulton does an excellent job of myth-busting. She also brings up the important issue of secrecy surrounding the PACE trial.

Why are documents pertaining to ME being locked up for 75 years?

My guess is that they are being buried to protect the reputations of the authors (and their institutions). The perpetuators of this crime against humanity will all be dead in 75 years - but their legacy, CBT and graded exercise therapy, will live on.

[The only "myth" in Sonia's article which is not an actual myth is that ME is not catching. ME got its name from the Royal Free outbreak. There have been 60 documented outbreaks of ME (including the one that saddled us with the name CFS). The word "outbreak" means that there is contagion.]

All in the mind? Why critics are wrong to deny the existence of chronic fatigue

By Sonia Poulton

Published: Mail Online. 10:15 Est, 8 May 2012, updated:16:49 EST, 8 May 2012

This week is Myalgic Encephalomyelitis Awareness Week or, as it's more accessibly referred to these days: M.E. That may not mean a great deal to you. Certainly, it didn't to me.

Oh wait, yes it did.

Based on no personal knowledge whatsoever - fortunately neither I or my loved ones have M.E. - my judgement was gleaned from how the world has portrayed the illness.

Like millions of others, I have seen M.E. through the eyes of the medical establishment, the Government and the Media. The picture has not been good.

Here is what I have previously understood about M.E. and those who have it.

M.E. sufferers are workshy malingerers. They whine, constantly, about feeling tired. They are annoying sympathy seekers.

Damn it. We're all tired. Especially those fools like me who work all hours God Sends (and even some he doesn't) to support the type of people who say they are too tired to work.

Oh, and mostly, importantly, M.E. is 'all in the head' and can be overcome with a bit more determination and a little less of the 'poor me' attitude.

That, generally, is what I thought about M.E.

Until, that is, a reader sent me a DVD of a British-made film about the illness titled 'Voices From The Shadows'.

I receive dozens of clips and films each month, and I try and see as many as I humanly can, but there was something about 'Voices...' that stopped me in my tracks.

One of the reasons the film had such an impact is because it challenged my deep-seated preconceptions about M.E.

Through 'Voices...' - and the subsequent research I have conducted - I have come to realise that what I thought I knew about the illness was a fallacy but, more importantly than that, was actually detrimental to those affected.

So, as a naturally curious individual (I'm not a journalist by mistake) I began to question why I had been furnished with one version of events - and inaccurate ones at that.

The more I began to delve into the subject the more curious it all became.

Like for example, why are records pertaining to ME locked away in our national archives in Kew for 75 years? The normal period would be 30 years.

75 years, the period generally used for documents of extreme public sensitivity and national security, is excessive.

The reason given, that of data protection, is a nonsense as it is perfectly acceptable, and easy, to omit names on official documents. The excuse, supplied in Parliamentary questions by the Department of Work and Pensions, didn't wash with me.

Why, I thought, were they making such an exception?

It got me thinking about what information the files actually do contain. And, seeing as the topic of M.E. is still beset with misunderstanding, we could all benefit from some enlightenment on the subject.

So, to this end - and seeing as it M.E. Awareness Week - here is my personal guide to shattering the myths and blatantly-pedalled untruths about M.E.

Myth No. 1: ME is a mental illness

Not so. It is a neurological one. It is not a case of 'mind over matter' despite many GP's and health professionals still thinking it is. Psychiatrists have bagged it as 'their thing' and the General Medical Council has been somewhat remiss in suporting it as a physical condition.

I spoke with one ME sufferer, who asked to remain anonymous for fear of upsetting the medical professionals who are currently treating her. She said a new GP at her practice had suggested she take up meditation to help her combat her decades-old condition.

Thankfully there are some doctors, few and far between admittedly, who really understand the physical nature of M.E.

Dr. Speight, a medical advisor for a number of M.E. charities does. Commenting on the wide-ranging debilitation of the illness, he has said:

'The condition itself covers a wide spectrum of severity but even the mildest cases deserve diagnosis and recognition because if they are given the wrong advice or don't handle themselves correctly they can become worse.

'At the more severe end of the spectrum there's a minority of patients who are truly in a pitiable state...some of them in hospitals, some of them at home...and this end of the spectrum is really one of the most powerful proofs to me of what a real condition this is and how it cannot be explained away by psychiatric reasons.'

Sadly, there are still many health professionals who buy into the notion that M.E. is a psychological disorder and should be treated as a form of insanity.

In Denmark, only last week, The Danish Board of Health sought to remove a 23-year old woman, Karina, from her family home on the grounds of mental illness despite the fact that what she really has is M.E.

Karina, bed-bound, light and sound sensitive and too weak to walk is considered to be insane, rather than physically sick, and her family has been repeatedly told by Danish doctors that the diagnosis of M.E. is not recognised.

Myth 2: ME is just extreme tiredness, right?

Wrong. Despite falling under the Chronic Fatigue Syndrome category - as does Fibromylgia which has its own Awareness Day next week - it is entirely wrong to assume that M.E. is merely about lack of energy.

This confusion arose over the past 20-odd years and is due to the condition being re-classified as a Fatigue Syndrome.

The result of this has been to trivialise the illness which has served as fodder for ill-informed public commentators who have used M.E. and Fibromylgia to talk about 'scroungers' in the benefits system who are 'too lazy' to get out of bed.

For those who know about the illness, this type of commentary is viewed as dangerous rhetoric that deserves to be classified as a form of hate crime.

Myth No. 3: M.E. is just like a bad flu

Oh, if only. M.E. is a complex, chronic, multi-system illness that affect the body in similar ways to Multiple Scelerosis. In addition, inflammation of the neurological system can lead to heart disease, extreme muscle pain and other debilitating and life-threatening conditions.

As one doctor put it, comparing M.E. to an illness like flu is like comparing Emphysema to a chest infection. It seriously undermines the truth extent of M.E.

Myth No. 4: M.E. sufferers should just 'pull themselves together'

Many sufferers have found themselves abandoned by health professionals, struck off of registers and even rejected by their own families when they have failed to respond to 'tough love'.

Too many people assume that M.E. can be overcome with the right mental attitude. This consequently leaves M.E. sufferers even more vulnerable to issues like depression as they are further isolated.

M.E. is not a case of the mind being able to heal itself with determination.

M.E. breaks the body down and that also includes the brain.

Myth No. 5: Only adults have M.E.

Children have M.E. and their childhoods are destroyed as a consequence.

Margaret Rumney of Allendale, Northumberland.watched as her 11-year-old daughter, Emma, was reduced to a shell of her former self when she was struck down with M.E. nine years ago.

"Since then it has been a continual rollercoaster of emotions and has been one fight after the other," says Margaret. "It is very hard for my daughter being ill, she is virtually housebound, often reliant on a wheelchair, and to have to cope with disbelief and ridicule on top of this makes this illness even harder to bear.

"Our experience of my daughter's school was an awful one. When my daughter was receiving home tuition organised officially by the Education Welfare Officer we were threatened by one professional that if my daughter didn't return to school that it would be classed as a psychological issue and social services would get involved."

Threats and intimidation of this nature at the hands of the authorities are a constant feature of those in the M.E. community, and particularly those caring for children with the illness.

Naturally, this pressure merely adds to the overall anxiety that sufferers are already experiencing. Education is key. Bullying is not.

Myth No. 6 - You can 'catch' M.E.

A hotly contested issue. Data suggests it's possible but the true cause is still subject to much debate among the more knowing professionals. What appears clear, however, is that ME seems to follow on from various viral infections, including meningitis. More research is needed.

Myth No. 7: Real M.E. sufferers are few and far between

There are currently 250,000 recognised cases of ME in the UK. That's 1 in 250 so that's hardly an insignificant number, is it?

Myth No. 8: Only severe cases of M.E. are worth acknowledging

Terrible misconception. M.E. ruins people's lives even if the patient is not entirely bedbound.

The media tend to concentrate on the worst case scenarios but this does not help the full situation as it leaves others, who are still able to move at times, with the stigmatisation of 'not being ill enough'.

Claire Taylor-Jones, a mother of one from Rhyl in North Wales, has been unable to pursue her ambition of becoming a solicitor after she was diagnosed with M.E.

In common with other sufferers, Claire has good days and bad days but she is not consistently well enough to pursue her goals and she is left in a type of limbo land. Her plans are on hold.

Myth No. 9: Children with M.E. have neglectful parents

There's the notion that children with M.E. are actually victims of mothers who have Munchausens by Proxy – the illness where parents act as if the child is sick to further their own need for attention.

This is a particularly dangerous belief system as it leaves the true M.E. sufferer without sufficient support and diagnosis and the carer is treated as the problem.

Myth No. 10: Physical exercise will benefit M.E. sufferers

Absolutely not true. Worse, still, enforced 'graded exercise' can escalate the condition to dangerous and irreparable levels for the patient.

During the research of this subject, I have watched footage of hospital physiotherapists literally bullying M.E. patients to stand and walk. It is pitiful to witness.

The physios say things like 'Come on, you can do it. You just have to put your mind to it' and, at worst, 'You're not trying hard enough.'

Julie-Anne Pickles, who has had M.E. for the past seven years has experienced a serious deterioration in her condition as a consequence of wrong diagnosis and ineffective medical response. She is now 90 per cent bedbound and has been diagnosed with depression, diabetes and Angina.

She told me:

"Cardiology phoned me with an appointment the other day and they told me to wear trainers because they want me running on a treadmill while on an ECG! I said: 'You do know I have M.E.?' They said they did but not to worry as I won't be running for more than five minutes! Running? I crawled on my hands and knees to the loo this morning!"

This idea among some of the medical professional that enforced exercise will help the condition of a M.E. belongs to a darker time in our history. A period when we thought that autistic children were a result of being born to cold and detached women or 'refrigerator mums' as they were heinously and immorally labelled.

Myth No. 11 - M.E. is not life-threatening

It is, although the true mortality rate of M.E. is mired in great confusion.

Recently, Labour MP George Howarth asked Paul Burstow, Minister of State for Care Services, to supply details of deaths to arise from M.E. Mr. Burstow replied that 'this information is not available and is not collected centrally'.

As with so many issues regarding our sick and disabled, the Coalition had this wrong, too.

According to figures obtained from the Office of National Statistics, there have been five deaths listed as the cause of M.E. in recent years.

For campaigners this is nothing less than a fudge of the true scale.

Figures are easy to massage with M.E. because it triggers so many other illnesses, such as heart disease. Given that many health professional still deny that M.E. is a physical condition, they are unable to list it as a cause of death even if it is.

Myth No. 12: M.E. is an excuse not to work

Despite recognition from the World Health Organisation in 1969 that M.E. is a neurological disorder, many Governments - including our present Coalition - have chosen to ignore this.

Consequently, M.E. sufferers are subject to a battery of controversial fit-to-work assessments. The anxiety and physical exertion this requires generally worsens the condition.

When the M.E. sufferer is unable to work, because of their illness, they are removed from disability benefit and are plunged into poverty.

So, for M.E. Awareness Week, let us be clear. M.E. is comparable to AIDS and cancer and all the other vicious and uncompromising diseases that savage the body and, in some extreme cases, kill it completely.

The fact that it is still so widely misunderstood is a modern day travesty that must be addressed without further delay. Or is it convenient that we still view M.E. as being 'all in the mind'?

I believe that we, as a nation, deserve to know the truth. Not only for those still battling the disease, but for those poor souls who have already been lost to it.

* For further details on Voices from the Shadows:

Thursday, May 8, 2014

The IOM, GWI, and Plausible Deniability

The Boston University School of Public Health study on Gulf War Illness (see below) is interesting for a couple of reasons, one of which is the proposed use of intranasal insulin to reduce neuroinflammation in veterans with GWI. Given the recent study confirming brain inflammation in patients with ME/CFS, and the substantial overlap in symptoms between the two illnesses, it doesn't require a leap of the imagination to put two and two together. If intranasal insulin helps vets with GWI, it may very well help people with ME/CFS.

Another interesting point this study raises is the absolute disjuncture between scientific research and the IOM's position on GWI. In the IOM's 2013 report on GWI, it stated that "Specific etiological agents are unknown...There is a growing belief that no specific causal factor or agent will be identified."

Studies linking GWI to pyridostigmine have been in circulation since the 1990s (Abou-Donia MB, Lotti M and Moretto A.). A 1999 article, "Nerve Gas Antidote a Possible Cause of Gulf War Illness" (Charatan), cited a 385-page report written by Dr. Beatrice Golomb, professor of medicine at the University of California and physician at the Veterans Affairs Medical Center, San Diego which concluded that "pyridostigmine bromide cannot be ruled out as a possible contributor to the development of unexplained or undiagnosed illness in some Gulf war veterans." (Update published in 2008) This report was submitted to the IOM, which rejected pyridostigmine bromide as a cause of GWI, as it had done previously. ("The epidemiologic data do not provide evidence of a link between PB and chronic illness in Gulf War veterans." IOM report, Gulf War and Health: Volume 1. Depleted Uranium, Pyridostigmine Bromide, Sarin, and Vaccines ( 2000 ), page 252)

Fourteen years later, the IOM continued to deny a connection between pyridostigmine bromide and GWI. It also denied a connection between the Gulf War and GWI, renaming it "chronic multisymptom illness."

If nothing else, the IOM has been consistent in its ability to whitewash reality.

If the IOM was able to ignore a 385-page report sponsored by the Rand Corporation, two decades of published research, and the testimony of Gulf War vets (to whom the IOM expressed appreciation for their "willingness ... to share their experiences and thoughts") they will certainly be able to turn a blind eye to two decades of research on ME/CFS. Like the Gulf War vets, they will freely acknowledge our suffering, but will ultimately turn a deaf ear to the "experiences and thoughts" of ME/CFS patients and those who care for them.

The question I have is this: Is having the IOM appear to "listen" worth the inevitable outcome? At what point do we stop accepting validation of our feelings as a legitimate response to the critical problems of having no FDA-approved treatment, virtually no NIH funding, and a definition that will continue to relegate us to the no-man's land of waste basket diagnoses?

Gulf War Illness: New Report Lauds Treatment Research, Confirms Toxic Causes

BU School of Public Health, April 28, 2014

Progress has been made toward understanding the physiological mechanisms that underlie Gulf War illness and identifying possible treatments, according to a report released Monday by a Congressionally mandated panel directed by a BU School of Public Health researcher.

Treatment research has increased significantly since 2008, and “early results provide encouraging signs that the treatment goals identified in the 2010 Institute of Medicine report are achievable,” the Research Advisory Committee on Gulf War Veterans’ Illnesses (RAC) said in a report presented to VA Secretary Eric Shinseki by the Committee’s scientific director, Roberta “Bobbie” White, chair of environmental health at BUSPH.

The Institute, part of the National Academies of Sciences, had forecast that “treatments, cures, and hopefully preventions” could likely be found with the right research.

The RAC report updates scientific research published since the Committee’s landmark report in 2008, which established that Gulf War illness was a real condition, affecting as many as 250,000 veterans of the 1990-91 Gulf War. The RAC Committee is composed of scientific experts and veterans.

“The conclusions of the 2008 RAC report had a substantial impact on scientific and clinical thinking about Gulf War illness, as well as the public acceptance of this disorder,” said White. The earlier report documented a number of studies that found evidence linking the illness to exposure to pesticides and pyridostigmine bromide (found in anti-nerve gas pills given to troops), as well as other toxic sources.

“Studies published since 2008 continue to support the conclusion that Gulf War illness is causally related to chemical exposures in the combat theater,” White said of the new report. “And many studies of the brain and central nervous system, using imaging, EEG and other objective measures of brain structure and function, add to the existing evidence that central nervous system dysfunction is a critical element in the disorder. Evidence also continues to point to immunological effects of Gulf War illness.”

Exposure to the nerve gas agents sarin and cyclosarin has been linked in several studies to changes in magnetic resonance imaging (MRI) that are associated with cognitive impairments — further supporting the nervous-system effects of those agents cited in the 2008 report.

“The Committee concludes that the evidence to date continues to point to alterations in central and autonomic nervous system, neuroendocrine, and immune system functions,” the report says.

Studies also continue to show that Gulf War illness is not associated with psychological stressors during the war, the panel said. Rates of PTSD and other psychiatric illnesses in Gulf War veterans are far below the rate of these disorders in veterans of other recent wars, and far below the rate of Gulf War illness.

In addition, the Committee said, new evidence has emerged suggesting that certain exposures may be linked to brain cancer in Gulf War veterans. Studies show that veterans who were most exposed to the release of nerve gas during the destruction of the Khamisiyah arms depot in Iraq have significantly elevated rates of death due to brain cancer.

Veterans who were exposed to the highest level of contaminants from oil well fires also have increased rates of brain cancer deaths, the report says.

The Committee encouraged studies exposing animals to toxic agents involved in Gulf War illness “because they can help to determine treatment targets in subgroups of veterans with specific exposures, for which there are known mechanistic pathways that cause illness and symptoms.”

In addition, “results from this work can be useful in protecting the health of future military personnel who will experience these exposures, as well as non-military populations with occupational or environmental exposures.”

The panel cited a number of “promising” treatment studies, including those testing certain dietary supplements, intranasal insulin, and continuous positive airway pressure to ease fatigue and pain and improve cognitive function.

A consortium of institutions led by BUSPH is studying markers in the blood and brain fluid, in addition to brain imaging (MRI and PET scans) and memory testing, to try to identify biomarkers of the condition. Studies also are planned on animals, to test initial treatments.

In a separate trial, BUSPH researcher Kim Sullivan and her colleagues are developing a possible treatment involving intranasal insulin, to target neuroinflammation. Researchers from the Boston VA Medical Center, the James J. Peters VA Medical Center in the Bronx, and the Icahn School of Medicine at Mount Sinai are involved in that trial, funded by a $1.7 million award from the Department of Defense.

While the RAC panel applauded an increase in the number of treatment studies funded by the Department of Defense’s Congressionally Directed Medical Research Program, it expressed grave concerns about a lack of research on other health problems and mortality among Gulf War veterans.

“Very little research” has been conducted to determine rates at which veterans have been affected by neurological diseases such as multiple sclerosis or Parkinson’s disease, cancers, and reproductive problems, the panel said.

“No comprehensive information has been published on the mortality experience of U.S. Gulf War era veterans after the year 2000,” according to the report.

Gulf War illness refers to the chronic symptoms that affect veterans of that conflict at markedly elevated rates, compared to other veterans’ groups and to the U.S. population as a whole. Symptoms can vary from person to person, but typically include some combination of widespread pain, headache, persistent problems with memory and thinking, fatigue, breathing problems, stomach and intestinal symptoms, and skin abnormalities.

Monday, May 5, 2014

Protocol for Disaster?

After reading the AHRQ study protocol, I was left with the distinct impression that they had already reached their conclusions, and the "systematic review" had simply been adjusted to fit them.

One question in particular had the undeniable scent of prior judgment:

"What harms are associated with diagnosing ME/CFS?"

This question undoubtedly refers to the CDC's refusal to include the 2-day CPET as part of their multi-site study. Beth Unger's justification for the exclusion was that the "physical toll would be too high" for patients.

But by the same token, the AHRQ review is designed to include the PACE trial. What kind of verbal gymnastics will the P2P perform in order to conclude that the 2-day CPET is harmful while simultaneously recommending GET?

Jennie Spotila has done an in-depth analysis of the review (below) which clarifies what is wrong with the review, and spells out the consequences.

Reprinted with permission

Protocol for Disaster?

By Jennie Spotila on OccupyCFS

The study protocol for the systematic review of ME/CFS was posted by the Agency for Healthcare and Research Quality yesterday.

It’s a recipe for disaster on its own, and within the broader context of the NIH P2P Workshop it’s even worse. Let me show you some of the reasons why.

Remind Me What This Is

The systematic evidence review is the cornerstone of the P2P process. The P2P meeting on ME/CFS will feature a panel of non-ME/CFS experts who will produce a set of recommendations on diagnosis, treatment, and research.

Because the P2P Panel members are not ME/CFS experts, they need background information to do their job. This systematic evidence review done by the Oregon Health & Science University under contract to AHRQ will be that background information. The systematic evidence report will be presented to the Panel in advance of the public P2P meeting, and will be used to establish the structure of the meeting as well.

The systematic review is the foundation. If done correctly, it would be a strong basis for a meaningful workshop. If done poorly, then everything that follows – the workshop and the resulting recommendations – will crumble. Based on the protocol published yesterday, I think “crumble” is putting it mildly.

The Key Questions
"You can’t get the right answer if you don’t ask the right questions."
 ~Dr. Beth Collins-Sharp, CFSAC Minutes, May 23, 2013, p. 12
As I wrote in January, the original draft questions for the evidence review included whether CFS and ME were separate diseases. That question is GONE, my friends. Now the review is only looking at two things:

  1. What methods are available to clinicians to diagnose ME/CFS and how do the use of these methods vary by patient subgroups?
  2. What are the benefits and harms of therapeutic interventions for patients with ME/CFS and how do they vary by patient subgroups?

These questions are based upon a single and critical assumption: ME and CFS are the same disease. Differences among patient groups represent subtypes, not separate diseases. The first and most important question is whether the ME and CFS case definitions all describe one disease. But they’re not asking that question; they have already decided the answer is yes.

The study protocol and other communications from HHS (including today’s CFSAC listserv message) state that the P2P Working Group refined these study questions. The implication is that since ME/CFS experts and one patient served on the Working Group, we should be satisfied that these questions were appropriately refined. But what I’m piecing together from various sources indicates that the Working Group did not sign off on these questions as stated in the protocol.

Regardless of who drafted these questions, they cannot lead to the right answers because they are not the right questions. And when you examine the protocol of how the evidence review will be conducted, these questions get even worse.

Protocol Problems

The real danger signals come from the description of how this evidence review will be done. The issue is what research will be included and assessed in the review. For example, when asking about diagnostic methods, what definitions will be considered?

This evidence review will include studies using “Fukada [sic], Canadian, International, and others“, and the Oxford definition is listed in the table of definitions on page 2 of the protocol. That’s right, the Oxford definition. Oxford requires only one thing for a CFS diagnosis: six months of fatigue. So studies done on people with long-lasting fatigue are potentially eligible for inclusion in this review.

The description of the population to be covered in the review makes that abundantly clear. For the key question on diagnostic methods, the study population will be: “Symptomatic adults (aged 18 years or older) with fatigue.” There’s not even a time limit there. Three months fatigue? Four? Six? Presence of other symptoms? Nope, fatigue is enough.

There is a specific exclusion: “Patients with other underlying diagnosis,” but which conditions are exclusionary is not specified. So will they exclude studies of patients with depression? Because the Oxford definition does not exclude people with depression and anxiety. We’ve seen this language about excluding people with other underlying diagnosis before – and it results in lumping everyone with medically “unexplained” fatigue into one group. This protocol is set up to result in exactly that. It erases the lines between people with idiopathic chronic fatigue and people with ME, and it puts us all in the same bucket for analysis.

And what about the key question on treatment? What studies will be included there? All of them. CBT, GET, complementary/alternative medicine, and symptom-based medication management. It’s not even restricted to placebo trials; trials with no treatment, usual care, and head-to-head trials are all included.

Let’s do the math. Anyone with unexplained fatigue, diagnosed using Oxford or any other definition, and any form of treatment. This adds up to the PACE trial, and studies like that.

But it’s even worse. The review will look at studies published since January 1988 because that was the year “the first set of clinical criteria defining CFS were published.” (page 6) Again, let’s do the math: everything published on ME prior to 1988 will be excluded.

Finally, notice the stated focus of the review: “This report focuses on the clinical outcomes surrounding the attributes of fatigue, especially post-exertional malaise and persistent fatigue, and its impact on overall function and quality of life because these are unifying features of ME/CFS that impact patients.” (page 2) In other words, PEM = fatigue. And fatigue is a unifying concept in ME/CFS. Did anyone involved in drafting this protocol actually listen to anything we said at last year’s FDA meeting?

Bad Science

Maybe you’re thinking it’s better for this review to cast a broad net. Capture as much science as possible and then examine it to answer the key questions. But that’s not going to help us in this case.

This review will include Oxford studies. It will take studies that only require patients to have fatigue and consider them as equivalent to studies that require PEM (or even just fatigue plus other symptoms). In other words, the review will include studies like PACE, and compare them to studies like the rituximab and antiviral trials, as if both patient cohorts were the same.

That assumption – that patients with fatigue are the same as patients with PEM and cognitive dysfunction – is where this whole thing falls apart. That assumption contaminates the entire evidence base of the study.

In fact, this review protocol makes an assumption about how the Institute of Medicine study will answer the same question. It is possible (though not assured) that IOM will design diagnostic criteria for the disease characterized by PEM and cognitive dysfunction. But this evidence review is based on an entirely different patient population that includes people with just fatigue. The conclusions of this evidence review may or may not apply to the population defined by the IOM.

It’s ridiculous!

But it’s the end use that really scares me. Remember that this systematic evidence review report will be provided to that P2P Panel of non-ME/CFS experts. The Panel will not be familiar with the ME/CFS literature before they get this review. And the review will conflate all these definitions and patient populations together as if they are equivalent. I think it’s obvious what conclusion the P2P Panel is likely to draw from this report.

I would love to be wrong about this. I would love for someone to show me how this protocol will result in GOOD science, and how it will give the P2P Panel the right background and foundation for the recommendations they will draft. Please, scientists and policy makers who read this blog – can you show me how this protocol will produce good science? Because I am just not seeing it.

What Do We Do?

This protocol is bad news but it is by no means the last word. Plans are already in motion for how the advocacy community can respond. I will keep you posted as those plans are finalized.

Make no mistake, this evidence review and P2P process are worse than the IOM study. We must respond. We must insist on good science. We must insist that our disease be appropriately defined and studied.

Thursday, May 1, 2014

What I Want for My Birthday

It's been a long, hard winter, but May is finally here, and soon I will be a year older. As it happens, this year I am sharing my birthday weekend with mothers  - and with Florence Nightingale.

Normally, I don't ask for anything for my birthday. The older I get, the less I need.

But this year there is something I want.


On the morning of Monday, May 12th I will be heading to the regional HHS headquarters in San Francisco to join a group of fellow demonstrators. We will set up a line of empty wheelchairs in front of the Federal Building at 90 Seventh Street, and we will place photos of people who have died of ME in those chairs. We will pin blue ribbons to our clothing, and hold up banners. Some of us will bring flowers and candles, and others will bring signs. We will deliver petitions to our representatives and to HHS.

At the same time, on the other side of the country, Mary Dimmock will be spreading the Banner of Hope on the lawn across from the Capitol Building in Washington, DC. The Banner is a 65-foot collection of pillow cases, each one made by someone with ME, bearing their name, dates of illness and artistic touches. It is a tribute to all those who have been bedridden by this disease.

If you are in the Bay Area, please join us in San Francisco. Contact:

If you are near Washington, join Mary at the Capitol. Contact:

Watch, Share, Tweet

Most of you who are reading this won't be able to be with us physically. But you can cheer us on, even from a distance. The San Francisco event will be live-streamed and posted on Youtube. You can watch it, and share it. You can tweet about both events.

You can help spread the word by liking the post about this event on my Facebook page. You can reprint this blog post. You can let the world know that Mary, and Susan, and Johannes, and Bobbi, and Erica, and all our friends will be standing there, representing a million people who can't.


You can write your Senators and Congressmen to let them know that you are ill, that your needs are not being served, and that you vote. Click HERE.

Say something like this:
I am a constituent who is ill with myalgic encephalomyelitis, also known as chronic fatigue syndrome. In spite of affecting over a million people in the US, this is a disease which has gotten very little funding over the past three decades. ME is not a benign disease. It has disabled hundreds of thousands of people in the US, and, in some of the more severe cases, has been fatal. The economic loss is calculated to be $17-23 billion dollars annually. Please ask NIH to allocate more funds to study this illness, and to help find a cure.
You can write a letter to the editor of your local newspaper. Tell them it is May 12th, and explain why this day is important to you.


You can join these Thunderclaps, and amplify our voices a hundred thousand times over.

Stop the IOM, Adopt the CCC

May 12th International Awareness Day

Tell the world! Today is May 12th International Awareness Day for ME/CFS & FM


You can light a candle, and remember that you are not alone.

That is what I want for my birthday.
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